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1 iled to rescue osteoclastogenesis or reverse osteopetrosis.
2 d has clinical implications for treatment of osteopetrosis.
3 anion exchanger member 2 (Slc4a2) results in osteopetrosis.
4          LysMCre;Ptpn11(fl/fl) mice had mild osteopetrosis.
5 conditionally deleted in osteoclasts develop osteopetrosis.
6 ted by many CLCN7 mutations underlying human osteopetrosis.
7 nts osteoclast differentiation, both causing osteopetrosis.
8 f AdIFNalpha to (NZB x NZW)F(1) mice induced osteopetrosis.
9 artment, with loss of ClC-7 function causing osteopetrosis.
10 ch as osteoporosis, rheumatoid arthritis and osteopetrosis.
11 lic bone diseases including osteoporosis and osteopetrosis.
12  osteoclast bone resorbing activity, causing osteopetrosis.
13 itf(mi/mi) and Bcl2(-/-) mice exhibit severe osteopetrosis.
14 states such as osteoporosis, or more rarely, osteopetrosis.
15 velopment in early-onset autosomal recessive osteopetrosis.
16 isruption of Atp6i in mice results in severe osteopetrosis.
17 egaly, and hypopigmentation, but neither had osteopetrosis.
18  alleles (mi/mi and Mior/Mior) in mice cause osteopetrosis.
19 l as neutrophilia disorders and the disease, osteopetrosis.
20  occur frequently in patients with malignant osteopetrosis.
21 ion and development, "HOD syndrome"), but no osteopetrosis.
22 ary defect in mice lacking the c-src gene is osteopetrosis, a deficiency in bone resorption by osteoc
23     Lack of mature osteoclasts caused severe osteopetrosis, a family of diseases characterized by imp
24 U.1-/- mice exhibit the classic hallmarks of osteopetrosis, a family of sclerotic bone diseases.
25       Defective osteoclast activity leads to osteopetrosis and bone marrow failure(1-9), whereas exce
26 sponding deficiencies in pycnodysostosis and osteopetrosis and identifies likely regulators of cathep
27 icient (RGS10-/-) mice that exhibited severe osteopetrosis and impaired osteoclast differentiation.
28 Deletion of Nfatc1 in young mice resulted in osteopetrosis and inhibition of osteoclastogenesis in vi
29 ause lysosome-related pathologies, including osteopetrosis and lysosomal storage.
30 ive mixed proximal-distal RTA accompanied by osteopetrosis and mental retardation is associated with
31                         Loss of ClC-7 causes osteopetrosis and mostly neuronal lysosomal storage.
32 orms of subunit a lead to the human diseases osteopetrosis and renal tubular acidosis.
33 trategies to rescue osteoclast deficiency in osteopetrosis and to modulate osteoclast activity in viv
34 or the osteosclerosis (oc) mutation includes osteopetrosis, and a variety of studies demonstrate that
35 d with a syndrome of renal tubular acidosis, osteopetrosis, and cerebral calcification.
36 or, muscle development, metabolic processes, osteopetrosis, and embryonic development.
37 processes, including renal tubular acidosis, osteopetrosis, and tumor metastasis.
38                          Autosomal recessive osteopetrosis (ARO) is a heterogeneous disorder, charact
39 ith severe bleeding, frequent infections and osteopetrosis at an early age.
40 rising result was that the animals developed osteopetrosis because of a defect in osteoclast differen
41 a soluble RANK-Fc fusion protein have severe osteopetrosis because of a reduction in osteoclasts, sim
42 beta3-integrins in beta3KOM mice resulted in osteopetrosis but had no effect on hemostasis or mortali
43 n mice decreases bone resorption, leading to osteopetrosis, but also increases the bone formation rat
44                                              Osteopetrosis can be partially treated by bone marrow tr
45 c, src-/- mice show only one major phenotype-osteopetrosis caused by an intrinsic defect in osteoclas
46  vivo, CD11b(+)-cre/Dicer-null mice had mild osteopetrosis caused by decreased osteoclast number and
47 , or stability, and that infantile malignant osteopetrosis caused by the R444L mutation in the human
48                           These mice develop osteopetrosis characterized by increased bone mass, redu
49 nic mice results in a profound yet nonlethal osteopetrosis, coincident with a decrease in later stage
50 n (BMT), which is commonly used in recessive osteopetrosis, could be used to treat ADO2, although the
51       Dysosteosclerosis (DSS) is the form of osteopetrosis distinguished by the presence of skin find
52       Src deficiency in mice leads to severe osteopetrosis due to a functional defect in osteoclasts,
53             Thus the findings reflect a mild osteopetrosis due to an intrinsic defect of osteoclastic
54 Glut1 deficiency in the progenitors leads to osteopetrosis due to fewer osteoclasts specifically in t
55       Deletion of Pyk2 in mice leads to mild osteopetrosis due to impairment in osteoclast function.
56 e NF-kappaB-inducing kinase (NIK), show mild osteopetrosis due to the inhibition of osteoclastogenesi
57 t mi allele and a PU.1 null allele developed osteopetrosis early in life which resolved with age.
58                                 In contrast, osteopetrosis has not been observed in a number of reces
59 terized by bleeding, frequent infections and osteopetrosis has now been attributed to mutations in th
60  hematopoietic transplantation for infantile osteopetrosis in 193 patients.
61 ss of Ostm1 leads to the most severe form of osteopetrosis in mice and humans.
62 hat ablation of Tak1 in myeloid cells causes osteopetrosis in mice as a result of defective osteoclas
63 emonstrate that myeloid NEMO deletion causes osteopetrosis in mice.
64 s in wild-type and src(+/-) mice and worsens osteopetrosis in src(-/-) mice by a novel mechanism, inc
65 nase-defective alleles of c-src also reduces osteopetrosis in src-/- animals and partially rescues a
66 dingly, deletion of Rbpj partially corrected osteopetrosis in Tak1-deficient mice.
67 bone homeostasis disorders of osteolysis and osteopetrosis in the same organism.
68 s in bone homeostasis, such as phenotypes of osteopetrosis in tibiae and osteolysis in calvariae as a
69 egion of 11q12-13 were found to be linked to osteopetrosis in two consanguineous Bedouin kindreds.
70 , Src251, lacking the kinase domain, induces osteopetrosis in wild-type and src(+/-) mice and worsens
71 n vivo and in cell culture, and induces mild osteopetrosis in young female PTPe KO mice.
72                                              Osteopetrosis is a genetic bone disease characterized by
73                                              Osteopetrosis is a heterogeneous group of bone disorders
74                          Autosomal recessive osteopetrosis is a rare congenital disorder characterize
75                                    Recessive osteopetrosis is caused by deficient osteoclast acid sec
76                              Their long bone osteopetrosis is largely reversed, and extensive medulla
77 ne regeneration and its mutation can lead to osteopetrosis, lysosomal storage disease and neurologica
78 d murine phenotypes, we tested whether human osteopetrosis maps to a region of conserved synteny.
79 t we term COMMAD, characterized by coloboma, osteopetrosis, microphthalmia, macrocephaly, albinism, a
80                                           An osteopetrosis mutation of ClC-7 displaying fast gating k
81                                          The osteopetrosis observed in these mice can be reversed by
82                            The fact that the osteopetrosis of CtsK-TLN1 and CtsK-Rap1 mice is substan
83 oduce dysfunctional osteoclasts resulting in osteopetrosis or osteosclerosis.
84 ne mass (osteoporosis), increased bone mass (osteopetrosis), or abnormalities in endochondral ossific
85 the absence of Roct expression results in an osteopetrosis phenotype in mice.
86 ted with the autosomal recessive syndrome of osteopetrosis, renal tubular acidosis, and cerebral calc
87  Their dysfunction causes Dent's disease and osteopetrosis, respectively.
88 ear cells from three infantile patients with osteopetrosis resulted in no significant activation of m
89 ANK(-/-) mice were characterized by profound osteopetrosis resulting from an apparent block in osteoc
90                    Mutant src(-/-) mice have osteopetrosis resulting from defective osteoclasts, the
91 ; surviving animals develop a severe form of osteopetrosis, resulting in extreme levels of splenic ex
92                                              Osteopetrosis results from a loss of ClC-7, but osteocla
93                                     Residual osteopetrosis, significantly delayed trabecular bone res
94  lymph node development and classic signs of osteopetrosis such as high bone mass and failure of toot
95 ut not recessive, mutations of mitf, produce osteopetrosis, suggesting a functional requirement for o
96 n a particularly malignant form of infantile osteopetrosis that is lethal in infancy, or early childh
97                           Autosomal dominant osteopetrosis type II (ADO2) is a heritable bone disease
98 -7(R760Q) , homologous to hClC-7(R762Q) , an osteopetrosis variant with fast gating kinetics, appeare
99  defects are secondary because of the severe osteopetrosis--we generated B cell-specific RANK knockou
100 mptoms of bleeding, frequent infections, and osteopetrosis, which are consequences of an inability to
101  cells, exemplified by bone diseases such as osteopetrosis, which frequently results from defects in
102 t, resulting in impaired bone remodeling and osteopetrosis, while hck-/- or fgr-/- mice have few and
103 rotegerin (OPG) in OPG transgenic mice cause osteopetrosis with normal tooth eruption and bone elonga
104 er syndrome, autosomal recessive syndrome of osteopetrosis with renal tubular acidosis, and familial
105 al body weight, limb size and fertility, and osteopetrosis with severity similar to that of RANK or R
106          TRANCE-deficient mice showed severe osteopetrosis, with no osteoclasts, marrow spaces, or to

 
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